Gas compression in lungs decreases peak expiratory flow depending on resistance of peak flowmeter

Pedersen, O. F., T. F. Pedersen, and M. R. Miller. Gascompression in lungs decreases peak expiratory flow depending onresistance of peak flowmeter. J. Appl.Physiol. 83(5): 1517-1521, 1997.It has recentlybeen shown (O. F. Pedersen T. R. Rasmussen, Ø. Omland, T. Sigsgaard, P. H. Quanjer, and M. R. Miller. Eur. Respir. J. 9: 828-833, 1996) that the addedresistance of a mini-Wright peak flowmeter decreases peak expiratoryflow (PEF) by ~8% compared with PEF measured by a pneumotachograph.To explore the reason for this, 10 healthy men (mean age 43 yr, range33-58 yr) were examined in a body plethysmograph with facilitiesto measure mouth flow vs. expired volume as well as the change inthoracic gas volume (Vb) and alveolar pressure(PA). The subjects performed forced vital capacity maneuvers through orifices of different sizes andalso a mini-Wright peak flowmeter. PEF with the meter and other addedresistances were achieved when flow reached the perimeter of theflow-Vb curves. The mini-Wright PEF meter decreased PEF from 11.4 ± 1.5 to 10.3 ± 1.4 (SD) l/s(P < 0.001),PA increased from 6.7 ± 1.9 to 9.3 ± 2.7 kPa (P < 0.001), anincrease equal to the pressure drop across the meter, and caused Vb atPEF to decrease by 0.24 ± 0.09 liter(P < 0.001). We conclude that PEF obtained with an added resistance like a mini-Wright PEF meter is awave-speed-determined maximal flow, but the added resistance causes gascompression because of increasedPA at PEF. Therefore, Vb at PEFand, accordingly, PEF decrease.

     

Effect of expiratory flow limitation on respiratory mechanical impedance: a model study

Peslin, R., R. Farré, M. Rotger, and D. Navajas.Effect of expiratory flow limitation on respiratory mechanicalimpedance: a model study. J. Appl.Physiol. 81(6): 2399-2406, 1996.Large phasicvariations of respiratory mechanical impedance (Zrs) have been observedduring induced expiratory flow limitation (EFL) (M. Vassiliou, R. Peslin, C. Saunier, and C. Duvivier. Eur. Respir. J. 9: 779-786, 1996). To clarify themeaning of Zrs during EFL, we have measured from 5 to 30 Hz the inputimpedance (Zin) of mechanical analogues of the respiratory system,including flow-limiting elements (FLE) made of easily collapsiblerubber tubing. The pressures upstream (Pus) and downstream (Pds) fromthe FLE were controlled and systematically varied. Maximal flow(max) increased linearly with Pus, was close to thevalue predicted from wave-speed theory, and was obtained for Pus-Pds of4-6 hPa. The real part of Zin started increasing abruptlywith flow () >85%max and either further increased or suddenlydecreased in the vicinity of max. The imaginary part of Zin decreased markedly and suddenly above 95%max. Similar variations of Zin during EFL were seenwith an analogue that mimicked the changes of airwaytransmural pressure during breathing. After pressure and measurements upstream and downstream from the FLEwere combined, the latter was analyzed in terms of a serial (Zs) and ashunt (Zp) compartment. Zs was consistent with a large resistance andinertance, and Zp with a mainly elastic element having an elastanceclose to that of the tube walls. We conclude that Zrs data during EFLmainly reflect the properties of the FLE.

     

Novel method for measuring effects of gas compression on expiratory flow

During forced vital capacity maneuvers in subjects with expiratory flow limitation, lung volume decreases during expiration both by air flowing out of the lung (i.e., exhaled volume) and by compression of gas within the thorax. As a result, a flow-volume loop generated by using exhaled volume is not representative of the actual flow-volume relationship. We present a novel method to take into account the effects of gas compression on flow and volume in the first second of a forced expiratory maneuver (FEV(1)). In addition to oral and esophageal pressures, we measured flow and volume simultaneously using a volume-displacement plethysmograph and a pneumotachograph in normal subjects and patients with expiratory flow limitation. Expiratory flow vs. plethysmograph volume signals was used to generate a flow-volume loop. Specialized software was developed to estimate FEV(1) corrected for gas compression (NFEV(1)). We measured reproducibility of NFEV(1) in repeated maneuvers within the same session and over a 6-mo interval in patients with chronic obstructive pulmonary disease. Our results demonstrate that NFEV(1) significantly correlated with FEV(1), peak expiratory flow, lung expiratory resistance, and total lung capacity. During intrasession, maneuvers with the highest and lowest FEV(1) showed significant statistical difference in mean FEV(1) (P < 0.005), whereas NFEV(1) from the same maneuvers were not significantly different from each other (P > 0.05). Furthermore, variability of NFEV(1) measurements over 6 mo was <5%. We concluded that our method reliably measures the effect of gas compression on expiratory flow.     

Influence of expiratory flow on closing capacity at low expiratory flow rates.

Single-breath oxygen (SBO2) tests at expiratory flow rates of 0.2, 0.5, and 1.01/s were performed by 10 normal subjects in a body plethysmograph. Closing capacity (CC)--the absolute lung volume at which phase IV began--increased significantly with increases in flow. Five subjects were restudied with a 200-ml bolus of 100% N2 inspired from residual volume after N2 washout by breathing 100% O2 and similar results were obtained. An additional five subjects performed SBO2 tests in the standing, supine, and prone positions; closing volume (CV)--the lung volume above residual volume at which phase IV began--also increased with increases of expiratory flow. The observed increase in CC with increasing flow did not appear to result from dependent lung regions reaching some critical "closing volume" at a higher overall lung volume. In normal subjects, the phase IV increase in NI concentration may be caused by the asynchronous onset of flow limitation occurring initially in dependent regions.     

Lymph flow from edematous dog lungs

We measured the flow rate (QLV) from cannulated lung lymph vessels in anesthetized dogs. Low-resistance lymph cannulas were used and the vessels were cannulated at the lung hilus. When we increased left atrial pressure to 42.9 +/- 5.7 (SD) cmH2O (base line = 6.6 +/- 4.6 cmH2O), the lungs became edematous and QLV increased from a base line of 20.4 +/- 21.5 microliters/min to 388 +/- 185 microliters/min. QLV plateaued at the higher level. We also measured the relationship between lymph flow rate and the height of the outflow end of the lymph cannula. From this relationship, determined at the end of the period of elevated left atrial pressure, we calculated the effective resistance and pressure driving lymph from the lungs. We also cannulated lymph vessels in the downstream direction and estimated the effective resistance and pressure opposing flow into the part of the lymphatic system between the lung hilus and the veins (extrapulmonary lymph vessels). We found that the effective resistance of the extrapulmonary part of the lymph system (0.042 +/- 0.030 (SD) cmH2O X min X microliter-1) was large compared with the resistance of the lymph vessels from the lungs (0.026 +/- 0.027). These data indicate that the resistance of the extrapulmonary part of the lung lymph system limits the maximum flow of lymph from edematous lungs.     

Modeling expiratory flow from excised tracheal tube laws.

Flow limitation during forced exhalation and gas trapping during high-frequency ventilation are affected by upstream viscous losses and by the relationship between transmural pressure (Ptm) and cross-sectional area (A(tr)) of the airways, i.e., tube law (TL). Our objective was to test the validity of a simple lumped-parameter model of expiratory flow limitation, including the measured TL, static pressure recovery, and upstream viscous losses. To accomplish this objective, we assessed the TLs of various excised animal tracheae in controlled conditions of quasi-static (no flow) and steady forced expiratory flow. A(tr) was measured from digitized images of inner tracheal walls delineated by transillumination at an axial location defining the minimal area during forced expiratory flow. Tracheal TLs followed closely the exponential form proposed by Shapiro (A. H. Shapiro. J. Biomech. Eng. 99: 126-147, 1977) for elastic tubes: Ptm = K(p) [(A(tr)/A(tr0))(-n) - 1], where A(tr0) is A(tr) at Ptm = 0 and K(p) is a parametric factor related to the stiffness of the tube wall. Using these TLs, we found that the simple model of expiratory flow limitation described well the experimental data. Independent of upstream resistance, all tracheae with an exponent n < 2 experienced flow limitation, whereas a trachea with n > 2 did not. Upstream viscous losses, as expected, reduced maximal expiratory flow. The TL measured under steady-flow conditions was stiffer than that measured under expiratory no-flow conditions, only if a significant static pressure recovery from the choke point to atmosphere was assumed in the measurement.     

Interdependence of regional expiratory flow

Flows from different lung regions interact at the junctions of the bronchial tree, and flow from each region depends on the driving pressures for other regions. At each junction, flow from the region with the higher driving pressure is favored. As a result there is a limit on the difference in alveolar pressures that can develop during expiratory flow from a lung with regional differences in lung compliance and airway resistance. The limiting pressure difference is smaller for lower flow. A nonuniform lung therefore empties more uniformly if it empties slowly, and maximum flow at low lung volume may be greater than it would be at the same lung volume during a maximal expiratory vital capacity maneuver.     

Positive effort dependence of maximal expiratory flow

The maximal expiratory-flow volume (MEFV) curve in normal subjects is thought to be relatively effort independent over most of the vital capacity (VC). We studied seven normal males and found positive effort dependence of maximal expiratory flow between 50 and 80% VC in five of them, as demonstrated by standard isovolume pressure-flow (IVPF) curves. We then attempted to distinguish the effects of chest wall conformational changes from possible mechanisms intrinsic to the lungs as an explanation for positive effort dependence. IVPF curves were repeated in four of the subjects who had demonstrated positive effort dependence. Transpulmonary pressure was varied by introducing varied resistances at the mouth but effort, as defined by pleural pressure, was maintained constant. By this method, chest wall conformation at a given volume would be expected to remain the same despite changing transpulmonary pressures. When these four subjects were retested in this way, no increases in flow with increasing transpulmonary pressure were found. In further studies, voluntarily altering the chest wall pattern of emptying (as defined by respiratory inductive plethysmography) did however alter maximal expiratory flows, with transpulmonary pressure maintained constant. We conclude that maximal expiratory flow can increase with effort over a larger portion of the vital capacity than is commonly recognized, and this effort dependence may be the result of changes in central airway mechanical properties that occur in relation to changes in chest wall shape during forced expiration.